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First published online 21 December 2006
doi: 10.1242/dev.02751

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Potency of testicular somatic environment to support spermatogenesis in XX/Sry transgenic male mice

Mayuko Ishii^1,*, Tsuyoshi Tachiwana^1,*, Anshin Hoshino^1,*, Naoki Tsunekawa¹, Ryuji Hiramatsu¹, Shogo Matoba¹, Masami Kanai-Azuma², Hayato Kawakami², Masamichi Kurohmaru¹ and Yoshiakira Kanai^1,

¹ Department of Veterinary Anatomy, The University of Tokyo, Yayoi 1-1-1, Bunkyoku, Tokyo 113-8657, Japan.
² Department of Anatomy, Kyorin University School of Medicine, Mitaka, Tokyo 181-8611, Japan.

Author for correspondence (e-mail: aykanai{at}mail.ecc.u-tokyo.ac.jp)

Accepted 20 November 2006

SUMMARY

The sex-determining region of Chr Y (Sry) gene is sufficient to induce testis formation and the subsequent male development of internal and external genitalia in chromosomally female mice and humans. In XX sex-reversed males, such as XX/Sry-transgenic (XX/Sry) mice, however, testicular germ cells always disappear soon after birth because of germ cell-autonomous defects. Therefore, it remains unclear whether or not Sry alone is sufficient to induce a fully functional testicular soma capable of supporting complete spermatogenesis in the XX body. Here, we demonstrate that the testicular somatic environment of XX/Sry males is defective in supporting the later phases of spermatogenesis. Spermatogonial transplantation analyses using XX/Sry male mice revealed that donor XY spermatogonia are capable of proliferating, of entering meiosis and of differentiating to the round-spermatid stage. XY-donor-derived round spermatids, however, were frequently detached from the XX/Sry seminiferous epithelia and underwent cell death, resulting in severe deficiency of elongated spermatid stages. By contrast, immature XY seminiferous tubule segments transplanted under XX/Sry testis capsules clearly displayed proper differentiation into elongated spermatids in the transplanted XY-donor tubules. Microarray analysis of seminiferous tubules isolated from XX/Sry testes confirmed the missing expression of several Y-linked genes and the alterations in the expression profile of genes associated with spermiogenesis. Therefore, our findings indicate dysfunction of the somatic tubule components, probably Sertoli cells, of XX/Sry testes, highlighting the idea that Sry alone is insufficient to induce a fully functional Sertoli cell in XX mice.

Key words: Sry, Sertoli cell, Transplantation, Spermatogenesis, Spermiogenesis, Mouse

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